The transcription factor NF-.kappa.B is key in regulating the expression of many genes involved in immune and inflammatory processes. In most cells NF-.kappa.B is present in the cytoplasm complexed with a member of the I.kappa.B family of proteins. I.kappa.B was originally identified as a labile factor which inhibited the activity of NF-.kappa.B by a directed protein-protein interaction. Two forms of the protein I.kappa.B-.alpha. and I.kappa.B-.beta., were purified from cytosolic fractions of human placenta (Zabel and Baeuerle, Cell 61:255-265, 1990) and at least three additional I.kappa.B family members have been described (Miyamoto and Verma, Adv. Cancer Res. 66:255-292, 1995). The activation of NF-.kappa.B upon cell activation is thought to involve the inducible phosphorylation of I.kappa.B family members on two N-terminal serines by a novel kinase prior to its degradation thereby allowing the free NF-.kappa.B to migrate to the nucleus where it binds to its consensus motif in target genes. Inhibition of either I.kappa.B phosphorylation or its degradation is known to inhibit the activition of NF-.kappa.B and thereby inhibit the expression of a number of immune and inflammatory mediators. This indicates that the I.kappa.B family has an established, proven history as therapeutic targets. Clearly there is a need for identification and characterization of further members of the I.kappa.B family which can play a role in preventing, ameliorating or correcting dysfunctions or diseases, including, but not limited to, inflammatory conditions including but not limited to rheumatoid arthritis, dermatosis (eg. psoriasis), inflammatory bowel disease, autoimmune diseases, tissue and/or organ rejection, Alzheimer's disease, stroke, atherosclerosis, restenosis, cancer, viral infection including but not limited to AIDS, osteoarthritis, osteoperosis, and Ataxia Telangiestasia.